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Angiology
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Two-Dimensional Echo Doppler Findings in Juvenile and Adult Onset Ankylosing Spondylitis with Long-Term Disease

F.J. Jiménez-Balderas

D. García-Rubi

S. Pérez-Hinojosa

J. Arellano

P. Yáñez

M.L. Sanchez

A. Camargo-Coronel

A. Zonana-Nacach

The authors' objective was to determine by 2-dimensional echo Doppler (2DECHO) the cardiac abnormalities in juvenile onset ankylosing spondylitis (JOAS) and adult onset ankylosing spondylitis (AOAS) in male patients with long-term disease. Twenty patients with JOAS, 31 with AOAS, and 20 healthy controls of the same age and gender without cardiopulmonary symptoms were studied. Using 2DECHO, the heart dimensions were determined according to American Society of Echocardiography guidelines. The left ventricle ejection fraction (LVEF) was calculated by Teichholz's formula. Cardiomyopathy was established when 2DECHO had diminished LVEF. Statistics used were the Student t and Fisher test, {chi}2, and ANOVA. Ninety percent of JOAS and 51 % of AOAS patients were B27+ (p = 0.005). The disease duration was 19.3 ±8.8 years in JOAS and 14.8 ± 12.8 years in AOAS (p = NS). Age at the time of the study was 30.7 ±9.9 years in JOAS vs 40.3 ± 12.7 in AOAS (p = 0.003), and vs 40.2 ± 17 years in controls (p = NS). There was a higher frequency of cardiomyopathy in AOAS (32.2%) than in JOAS (25%) and the controls (0%) (p = 0.01). Patients with JOAS had a higher mitral valve gradient (25%) than AOAS patients (19%, p = NS) and controls (0%, p = 0.04). Abnormal aortic ring reflectance was shown in 19% of AOAS vs 0% abnormalities in JOAS and controls (p = 0.01). The aortic root diameter was increased in 58% of AOAS, 30% of JOAS, and 0% of controls (p = 0.001).

The frequency of 2DECHO abnormalities was increased in cardiopulmonary asymptomatic spondylitis patients. Despite the high frequency of B27+, JOAS had a lower frequency of aortic abnormalities than AOAS. Mitral valve gradient was found in JOAS and in AOAS that could contribute to a decreased ejection fraction and to left ventricular dysfunction.

Angiology, Vol. 52, No. 8, 543-548 (2001)
DOI: 10.1177/000331970105200806


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